Ameliorative effects of wine-steamed Songaria Cynomorium Herb: Chemical characterization by UPLC-Q-TOF-MS and modulation of pathophysiology and JAK/STAT signaling pathway in kidney-Yang deficient rats.

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Tác giả: Yang Chen, Xiutong Ge, Shiru Jiang, Li Li, Wenjing Ren, Ji Shi, Gui Xu, Fan Zhang, Shuo Zhang, Jiahui Zhao, Yue Zhou

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: Netherlands : Fitoterapia , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 708309

Songaria Cynomorium Herb (SCH), a traditional Chinese medicinal herb, is recognized for its dual role as both a dietary supplement and a therapeutic agent. It is traditionally reputed to have kidney-tonifying and Yang-strengthening effects, which have made it a common ingredient in nutritious food supplements and health products. This study investigates the underlying mechanisms by which wine-steamed SCH, enhances kidney aphrodisiac qualities, focusing on the tyrosine kinase/signal transduction and transcriptional activation factor (JAK/STAT) signaling pathway. Ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS) was employed to qualitatively analyze the chemical constituents of SCH both before and after the wine-steaming process, and the significant differential components were screened out. A kidney-Yang deficiency model was induced by intragastric administration of hydrocortisone. Subsequently, the rats were treated with either raw SCH (RSCH) or wine-steamed SCH (WSCH) medicinal solutions. Urine output, organ indices, target gland axis-related indices, and renal tissue lesions were recorded and statistically compared between the treatment and control groups. RT-qPCR and Western blot analysis were utilized to assess the mRNA and protein expression levels of the JAK/STAT pathway and HIF-1α in the renal tissues of the animals. The results indicated that the chemical composition of the SCH underwent changes before and after the steaming process. The tonifying effects observed were more pronounced with WSCH than with RSCH, suggesting that the mechanism involves the inhibition of the JAK/STAT pathway and the downregulation of HIF-1α expression.
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